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This review analyses the rationale for combining venetoclax with inhibitors of histone deacetylase (HDAC). Class I histone deacetylase 1\/2\/3\u2010dependent suppression of myeloid cell leukaemia 1 and de\u2010repression of pro\u2010apoptotic BCL\u20102 homology domain 3 (BH3)\u2010only genes provide the strongest mechanistic basis, whereas HDAC6\/heat shock protein 90, autophagy, immune\u2010modulatory and super\u2010enhancer mechanisms remain context\u2010dependent and incompletely validated in primary AML under venetoclax exposure. Effects of HDAC inhibition must also be interpreted in the context of tumour protein 53 status. Early HDAC inhibitor\u2010containing composite regimens, particularly chidamide\u2010based CACAG\u2010VEN (chidamide, venetoclax, azacitidine, low\u2010dose cytarabine, aclarubicin and granulocyte colony\u2010stimulating factor), report high response rates, including overall response rate of 76.5\u201398.0%, complete remission\/complete remission with incomplete count recovery or composite complete remission of 73.5\u201393.3%, and measurable residual disease negativity of 44\u201361%. This six\u2010component regimen does not isolate the contribution of HDAC inhibition. Future development should prioritise biomarker\u2010selected trials that hold non\u2010HDAC components constant, incorporate pharmacodynamic HDAC engagement and BH3 profiling, and account for cytochrome P450 3A\u2010mediated drug interactions. 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